The for all that are concerned. This subsequent

 

 

The world shuns
those who are labelled abnormal. Once a person is diagnosed with any kind of
psychological state, their life and their loved one’s lives are forever
changed. As much as any medical illness, Schizophrenia presents suffers with an
enormous array of social, biological and economic conundrums. It also confronts
us with profound human suffering, for it involves alternations in the core of a
person’s subjectivity.

Somebody that has
schizophrenic disorder suffers in several areas of their life; but, the medical
and psychological communities are fighting for the understanding and freedom
for all that are concerned. This subsequent essay is a brief over read of the Psychotic disorder schizophrenic
disorder, the way the disorder affects people who suffer, and therefore the research
that continues to fight for a cure.  Schizophrenia
is a very common form of psychotic disorder (severe mental illness). It’s
lifetime prevalence is almost 1% it’s annual incidence is about 10-15 per 100,000,
and in the UK the average general practitioner cares for 10-20 schizophrenia
patients depending on the location and social surroundings of the practice (Davies, T., & Craig, T. K. (2009).

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Schizophrenia is
one of the most controversial psychiatric diagnoses. Over time, there has been
debates whether a distinct state of schizophrenia exists, whether it results
from genetic or environmental causes and whether it should be treated by using drug
therapy, electroconvulsive therapy, or more social and psychological
approaches.

The condition now
labelled as schizophrenia was first described by Kraepelin (1883,1981) using the
term dementia praecox. This label was chosen to show that it was a progressive and
deteriorating illness with no return to pre-morbid levels of functioning. After
some time, Bleuler (1908) identified four fundamental symptoms of what he
termed the group of schizophrenias ‘split mind’ ambivalence, disturbance of
association, disturbance of mood and fantasy over reality.

The exact cause
of schizophrenia remains hotly disputed. However, the consensus view is that it
comprises many related disorders characterized by fundamental distortions of
thinking and perception. Disturbance in thought process is one of the most
obvious symptoms of schizophrenia.

Symptoms are termed
‘positive’ or ‘negative’ depending on whether they are psychological add-ons
e.g. delusions or deficits e.g. anhedonia.  Such that it is a syndrome with various
presentations and variable, often relapsing, long term course. Although
schizophrenia is sometimes misconceived as ‘split personality’, the diagnosis
has great reliability over all even across any ages or cultures.

Symptoms of
schizophrenia are characterised most usually only as positive or negative,
although the traditional diagnostic subcategories as hebephrenic, paranoid, catatonic
and simple have mixtures of both.

Positive symptoms and signs

Hallucinations

These are perceptions
that occur without an appropriate sensory input. Although hallucinations can
occur in any sensory form – auditory (sound), visual (sight), tactile (touch),
gustatory (taste), and olfactory (smell) – hearing voices that other people do
not hear is the most common type of hallucination. The hallmark of
schizophrenia is that patients experience voices talking about them as ‘he’ or ‘she’
(third person auditory hallucinations). But second person ‘command’ voices also
occur, as do olfactory, tactile both somatic and visceral and visual hallucinations.

Delusions

Delusions are
abnormal beliefs held with absolute certainty, dominating the patient’s mind,
and untenable in terms of the sociocultural background. Delusions are often deriving
from attempts to make sense of other symptoms such as experience of passivity
(sensing that someone or something is controlling one’s body, emotions or
thoughts). For example, individuals experiencing paranoid type symptoms roughly
about one – third of people diagnosed with schizophrenia – often have delusions
of persecution or false and irrational beliefs that they are being cheated, harassed,
poisoned or conspired against. These people may believe that they, or a member
of their family or someone close to them, are the focus of this persecution. In
addition, delusion of grandeur, in which a person may believe he or she is
famous or important figure, may occur. However, such false beliefs are often
very difficult to challenge. Sufferers are frequently able to defend their
deluded beliefs in a coherent way and unable to understand that other people
find their delusional beliefs implausible (McGuire, Junginger, Adams, Burright
et al.. 2001).

Disorganised
speech and thought behaviour

Psychotic symptoms
frequently exhibit a range of attributes that show disordered thinking and disordered
speech.

World Salad:
language of person experiencing a psychotic episode appears so disorganised
that there seems to be no link between one phrase and the next. This is known
as word salad. Some word salads simply do not seem to be attempts to communicate
anything structured and appear to drift without substance from one unconnected
sentence to the next.

Neologisms: Making
up words and use them in their attempts to communicate. These are constructed
by condensing or combining several words.

Clanging: trying
to communicate by using words that rhyme.

Disorder of motor
behaviour

People suffering
from psychosis can also exhibit a number of problems associated with disorders
of motor behaviour, although these types of symptoms are usually found within
more severe cases and chronic cases of psychosis. The actual two most common
motor symptoms include stereotypy and catatonic stupor.

Stereotypy:
indicates reduced purposeful control of behaviour. During stereotypy,
individuals repetitively indulge in the same motor behaviour pattern. Examples of
this include head rubbing, agitated pacing backwards and forwards, repetitive
smacking or patting of parts of the body or repetitive manipulation of an
object.

Catatonia: people
may lapse into a catatonic stupor. Those who lapse into this state become withdrawn
and inactive for long periods. Individual will adopt a rigid, often awkward
posture for many hours. Others exhibit what is known as waxy flexibility, and
will maintain a posture into which they have been placed by someone else.

Other symptoms 

sometimes present in schizophrenia but not often
enough to be definitional alone include affect inappropriate to the situation
or stimuli, unusual motor behaviour (pacing, rocking), depersonalization,
derealization, and somatic preoccupations.

Negative Symptoms

A negative
symptom is the absence of some ability or attribute a normal person would
possess. These include loss of personal abilities such as initiative, interest
in others and the sense of enjoyment (anhedonia). Blunted or fatuous emotions
(flat affect), limited speech and much time spent doing nothing are typical behaviours.
Subtle cognitive deficits often persist or even worsen despite continuing
treatment.

Affective
flattening

 is the reduction in
the range and intensity of emotional expression, including facial expression,
voice tone, eye contact, and body language.

Alogia

or poverty of speech, is the
lessening of speech fluency and productivity, thought to reflect slowing or
blocked thoughts, and often manifested as short, empty replies to questions.

Avolition

 is the reduction, difficulty, or inability to
initiate and persist in goal-directed behaviour; it is often mistaken for
apparent disinterest. (examples of avolition include: no longer interested in
going out and meeting with friends, no longer interested in activities that the
person used to show enthusiasm for, no longer interested in much of anything,
sitting in the house for many hours a day doing nothing.)

 

However,
the signs and symptoms depend on person to person, both in severity and form.
Not every person will show all the symptoms and possibly the symptoms could
also change over time. The effects can be extremely hard on both the person
with the disorder and for those people who are around them when the signs and
symptoms of schizophrenia are ignored or not treated well.

Schizophrenia is usually treated with an
individually tailored combination of therapy and medication.  Early
treatment with ‘antipsychotic drugs’ , minimising the duration of untreated
psychosis is the central to resolving unpleasant symptoms and social
impairment. National Institute for health and clinical excellence guidelines recommend
‘atypical’ antipsychotics as first line of treatment ( i.e. Olanzapine (Zyperexa), Risperidone (Risperdal) and Quetiapine), although they are probably
no more effective than the traditional dopamine blockers (e.g. Haloperidol, Chlorpromazine
(Largactil or Thorazine)). Only
Risperidone is available as a depot preparation and they vary in their sedating
properties, weight gain and hyperglycaemia.

 These
are examples of newer versions which are often referred as second-generation
antipsychotics which can work quickly in comparison to other medication. You may only need antipsychotics until your acute
schizophrenic episode has passed. Furthermore, besides the medication,
psychological interventions are also important in treating schizophrenia.
Psychological interventions are based on cognitive behavioural therapy (CBT),
which for many patients can reduce the impact of hallucinations and delusional
beliefs, the use of insight orientated psychoeducation for patients and carers
and family work.

Relapse in
schizophrenia seems closely associated with the level of the family’s emotional
expression as measured by formal assessments of critical comments or expressed hostility
in family interviews. Fashionable theories of causation in the 1960s which
designated the ‘schizophrenogenic’ parent, have now been discarded. However, a
close association between high arousal in the family and early relapse: this
can be lowered by structured family education, reducing face to face contact via
attendance at a day centre and formal family therapy.

In the past and
still currently one of the most important idea was that the dopamine system expressively
accounted for schizophrenic symptoms present in patients, by activation of the
dopamine receptors. Also, the biological approach to treatment of schizophrenia
consists of drug therapy by giving patients antipsychotic drug such as clozapine
or haloperidol which will then target to block dopamine receptors. Using antipsychotics
is only seen as effective in treating the positive symptoms (behaviour or thoughts,
such as hallucinations or delusions), while having a limited effect on the negative symptoms (a withdrawal or lack of function that you would not usually expect to see
in a healthy person; for example, people with schizophrenia often appear
emotionless and flat) (Chavez et a..2009).

Some of the typical
antipsychotic drugs causes side effects, such as tardive dyskinesia, and
symptoms which includes unusual facial and body movements, these occur as a
result of the blockage of D2 receptors (Remington,
2003; Horacek et al., 2006). Atypical antipsychotic drugs given in clinically effective
dosages don’t give these side effects (Leucht et al., 1999; Seeman, 2002) because
they don’t act directly on the dopamine receptors. Some studies have shown that
atypical are effective on negative symptoms, cognitive dysfunction and
aggression (Remington, 2003). Researchers have also said the real cause for
this is that atypical antipsychotics such as clozapine have lower affinities
for D2 receptors and bind loosely to the receptors when released (Horacek et
al., 2006; Seeman, 2002), than antipsychotics such as haloperidol.

60-80%
of D2 receptors are occupied by antipsychotic drugs in the brain of the
patient. Whereas Clozapine and Quetiapine take about 0-50% (Seeman, 2002).
Clozapine acts as partial agonists at glycine modulating site of NMDA, lower concentration
increases depolarisation and higher concentration inhabits depolarisation which
is why clozapine works better than others.

Antipsychotics
affect glutamatergic activity in a lot go ways, such as improving the release
of glutamate in the striatum, changing the density of glutamate and directly
linking with BMDA receptors. New clinical trials show NMDA receptors activity
improved by drugs affecting the glycine modulatory site of NMDA receptor which
have shown decreased negative symptoms and improved cognitive function (Goff and Coyle, 2001).

Glutamatergic
neuron is linked with limbic system, cortex and thalamus. These are implicated
in schizophrenia. Therefore, some researchers proposed the idea pf glutamate
system in treating schizophrenia. Diminished activation of NMDA receptors is because
of schizophrenia. Psychosis models were induced in the cognitive deficits and negative
symptoms are much better than the dopamine (Krystal et al., 1994; Hashimoto et
al., 2003).

Haloperidol,
synaptic plasticity is great to document the striatum with highest
concentration of D2 receptors (Horacek et al,2006). It has also been shown in
few studies that blockage of D2 receptors doesn’t reduce the symptoms of memory
impairments, therefore, it has been advised that direct modulation of
hyperactive NMDA by drugs may allow us to target microcircuits within the mesocratic,
which cannot be accessed by D2 based treatments (Paz et al..,2008).

Acamprosate acts like an antagonist when the NMDA receptors
are stimulated but acts as a agonist when the NMDA receptors stimulation is
minimal. It has been predicted that this can enhance the functions of NMDA
receptors in schizophrenia and improve cognition. (Tuominen et al, 2005)
published a review/meta-analysis and found out that D-Serine and glycine was
successful in reducing negative symptoms. There was no big effect of d-serine
or glycine on the positive symptoms. Therefore (Shim et al..2008) also said
that some other drugs could be effective by acting on other sites of NMDA
receptors in the treatment of Schizophrenia as research in glutamatergic drugs.

Minocycline is another drug used
to see for any possible effects in treating symptoms of the condition. The exact
mechanism of action of minocycline is unclear, some recent research shows that
it doesn’t modulate the glutamatergic system. In animal studies, it is reversed
several NMDA r antagonist transmissions (Goff and Coyle, 2001).

 

In conclusion it is now suggested that dysfunction of
glutamatergic neurotransmission takes a huge part in treating the symptoms of
schizophrenia especially in negative a cognitive impairment and it is a good
target for drug development (Goff and Coyle, 2001).

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